ReviewClinical and molecular hepatology2012
Hepatitis C virus and hepatocarcinogenesis.
Review in Clinical and molecular hepatology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
41 citing papers in PubMed, 99 citations in OpenAlex.
- lncRNAs as Biomarkers of Hepatocellular Carcinoma Risk and Liver Damage in Advanced Chronic Hepatitis C.Current issues in molecular biology · 2025Article
- Hepatocellular carcinoma risk decreases as time accrues following hepatitis C virus eradication.Alimentary pharmacology & therapeutics · 2024Article
- Murine leukemia virus (MLV) P50 protein induces cell transformation via transcriptional regulatory function.Retrovirology · 2023Article
- The care cascade for hepatitis C virus and prognosis of chronic hepatitis C patients treated with antiviral agents in a tertiary hospital.BMC gastroenterology · 2023Article
- Massive Hepatocellular Carcinoma with Situs Inversus Totalis Achieved a Complete Response Following Camrelizumab Plus Apatinib and Combined with Two-Stage Hepatectomy: A Case Report.Pharmacogenomics and personalized medicine · 2023Article
- Hepatitis B virus X protein and hepatitis C virus core protein cooperate to repress E-cadherin expression via DNA methylation.Heliyon · 2022Article
- HCV and tumor-initiating stem-like cells.Frontiers in physiology · 2022Review
- Role of Histone Post-Translational Modifications in Inflammatory Diseases.Frontiers in immunology · 2022Review
- Correlation of hepatitis C virus-mediated endoplasmic reticulum stress with autophagic flux impairment and hepatocarcinogenesis.Medical molecular morphology · 2021Article
- Article
- Microbiome in human cancers.Access microbiology · 2021Review
- Long non-coding RNAs (LncRNAs), viral oncogenomics, and aberrant splicing events: therapeutics implications.American journal of cancer research · 2021Review
- Review
- Review
- A comprehensive genome-wide profiling comparison between HBV and HCV infected hepatocellular carcinoma.BMC medical genomics · 2019Article
- MicroRNA-548b inhibits proliferation and invasion of hepatocellular carcinoma cells by directly targeting specificity protein 1.Experimental and therapeutic medicine · 2019Article
- Cellular Gene Expression during Hepatitis C Virus Replication as Revealed by Ribosome Profiling.International journal of molecular sciences · 2019Article
- Integrating the Epigenome to Identify Drivers of Hepatocellular Carcinoma.Hepatology (Baltimore, Md.) · 2019Article
- Hepatitis C Virus Downregulates Ubiquitin-Conjugating Enzyme E2S Expression To Prevent Proteasomal Degradation of NS5A, Leading to Host Cells More Sensitive to DNA Damage.Journal of virology · 2019Article
- Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hepatitis C virus (HCV) is an RNA virus that is unable to integrate into the host genome. However, its proteins interact with various host proteins and induce host responses. The oncogenic process of HCV infection is slow and insidious and probably requires multiple steps of genetic and epigenetic alterations, the activation of cellular oncogenes, the inactivation of tumor suppressor genes, and dysregulation of multiple signal transduction pathways. Stellate cells may transdifferentiate into progenitor cells and possibly be linked to the development of hepatocellular carcinoma (HCC). Viral proteins also have been implicated in several cellular signal transduction pathways that affect cell survival, proliferation, migration and transformation. Current advances in gene expression profile and selective messenger RNA analysis have improved approach to the pathogenesis of HCC. The heterogeneity of genetic events observed in HCV-related HCCs has suggested that complex mechanisms underlie malignant transformation induced by HCV infection. Considering the complexity and heterogeneity of HCCs of both etiological and genetic aspects, further molecular classification is required and an understanding of these molecular complexities may provide the opportunity for effective chemoprevention and personalized therapy for HCV-related HCC patients in the future. In this review, we summarize the current knowledge of the mechanisms of hepatocarcinogenesis induced by HCV infection.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.